The general goal of this study is to establish the factual link between visual cortical plasticity and the central monoamine system in the developing brain. We will explore, in particular, ways to modify cortical plasticity by direct manipulation of monoaminergic receptors within the visual cortex. For this purpose, various receptor antagonists or agonists will be delivered continuously through a chronically implanted microperfusion system. A converse approach with stimulation of the ascending NE pathways in the brain stem, in place of cortical cannulae, will also be taken to study the perfectly normal cortex. Changes in the extent of binocular convergence of individual visual cortical cells will be used as a measure for neuronal plasticity in the visual cortex which receives various forms of visual experience including the normal one and monocular lid suture. As an extension of an initial study which we have completed recently, more effort will be made to elucidate morphologically the nature of monoamine-containing nerve terminals in the visual cortex of kittens and adult cats. Both catecholamine histofluorescence and electron microscopy will be employed for this part of the work. A particular question we wish to answer is the apparently low incidence of synapse formation by catecholamine terminal boutons in the cerebral cortex. We will use the early sign of degeneration in 6-OHDA treated cortex as a marker of catecholamine-containing boutons which can be thus identified in glutaraldehyde fixed tissues.